Well, this is really about alcohol consumption in general, coupled with, I hope, a decent review of the underlying mechanisms of what happens psychologically and chemically.
I will be covering the biochemistry in several aspects. The metabolism of ethanol is central to this. Some ethanol is produced by bacteria in the gut, so everyone has, at the very least, a low level of ethanol metabolism. Once ethanol is consumed, it then begins being oxidized by an alcohol dehydrogenase. This enzyme converts ethanol into acetaldehyde. Acetaldehyde is a much more directly toxic substance. Acetaldehyde is then converted to acetic acid which is then converted to acetyl-CoA. At each step of this, the substances have physiological effects on the body which I shall briefly discuss.
Ethanol is an allosteric modulator of GABAA. Since GABAA is an inhibitory neurotransmitter receptor, which causes a decrease in neuron firing, GABAA is essentially a depressant receptor. Continuous activation of GABAA results in it being downregulated to allow for the nervous system to function properly. This is what partially causes alcohol tolerance and physical dependence. Complete withdrawal from alcohol after prolonged heavy use can result in uncontrolled synapse firing. (siezure, convulsion, etc.)Some medications can reduce this hypersensitivity of neurons. This is why severe alcoholics generally must undergo “detox” to treat these physiological effects of alcohol dependence prior to a therapy to prevent relapse.
Acetaldehyde is one compound which contributes to hangovers and is partially responsible for the damage associated with alcohol consumption. It has been hypothesized that cirrhosis may partially be due to acetaldehyde. Additionally, prolonged use of alcohol results in fatty deposits in the liver, although the exact mechanism of this is unknown. Acetaldehyde also is a potent carcinogen and mutagen which is partially responsible for many of the cancer and disease risks associated with smoking, car exhaust, and alcohol consumption.
As for the beneficial effects of ethanol consumption in low to moderate levels (less than two drinks per day), there is good evidence that this is the case. These include a decreased incidence of cardiovascular disease and some protection from some infectious diseases and diabetes. In higher levels, however, these benefits seem to be countered by greater than two drinks per day. The optimal point of mortality associated with alcohol is near the one drink per day mark.
As for the physiological effects of alcohol withdrawal, these are slightly more complex. The most severe of the symptoms are anorexia, delirium tremens, diarrhea, hyperthermia, nausea, seizures, sweating, and tachycardia. All of these are due to the overexcited state of neurons. Typically given to suppress these effects are a range of GABA modulators such as benzodiazepines, Carbamazepine, and Flumazenil. These medications are typically given due to the ease which these can be metered.